Peri-operative SARS-CoV-2 infection increases postoperative mortality. The aim of this study was to determine the optimal duration of planned delay before surgery in patients who have had SARS-CoV-2 infection. This international, multicentre, prospective cohort study included patients undergoing elective or emergency surgery during October 2020. Surgical patients with pre-operative SARS-CoV-2 infection were compared with those without previous SARS-CoV-2 infection. The primary outcome measure was 30-day postoperative mortality. Logistic regression models were used to calculate adjusted 30-day mortality rates stratified by time from diagnosis of SARS-CoV-2 infection to surgery. Among 140,231 patients (116 countries), 3127 patients (2.2%) had a pre-operative SARS-CoV-2 diagnosis. Adjusted 30-day mortality in patients without SARS-CoV-2 infection was 1.5% (95%CI 1.4-1.5). In patients with a pre-operative SARS-CoV-2 diagnosis, mortality was increased in patients having surgery within 0-2 weeks, 3-4 weeks and 5-6 weeks of the diagnosis (odds ratio (95%CI) 4.1 (3.3-4.8), 3.9 (2.6-5.1) and 3.6 (2.0-5.2), respectively). Surgery performed ≥ 7 weeks after SARS-CoV-2 diagnosis was associated with a similar mortality risk to baseline (odds ratio (95%CI) 1.5 (0.9-2.1)). After a ≥ 7 week delay in undertaking surgery following SARS-CoV-2 infection, patients with ongoing symptoms had a higher mortality than patients whose symptoms had resolved or who had been asymptomatic (6.0% (95%CI 3.2-8.7) vs. 2.4% (95%CI 1.4-3.4) vs. 1.3% (95%CI 0.6-2.0), respectively). Where possible, surgery should be delayed for at least 7 weeks following SARS-CoV-2 infection. Patients with ongoing symptoms ≥ 7 weeks from diagnosis may benefit from further delay.

SARS-CoV-2 has been associated with an increased rate of venous thromboembolism in critically ill patients. Since surgical patients are already at higher risk of venous thromboembolism than general populations, this study aimed to determine if patients with peri-operative or prior SARS-CoV-2 were at further increased risk of venous thromboembolism. We conducted a planned sub-study and analysis from an international, multicentre, prospective cohort study of elective and emergency patients undergoing surgery during October 2020. Patients from all surgical specialties were included. The primary outcome measure was venous thromboembolism (pulmonary embolism or deep vein thrombosis) within 30 days of surgery. SARS-CoV-2 diagnosis was defined as peri-operative (7 days before to 30 days after surgery); recent (1-6 weeks before surgery); previous (≥7 weeks before surgery); or none. Information on prophylaxis regimens or pre-operative anti-coagulation for baseline comorbidities was not available. Postoperative venous thromboembolism rate was 0.5% (666/123,591) in patients without SARS-CoV-2; 2.2% (50/2317) in patients with peri-operative SARS-CoV-2; 1.6% (15/953) in patients with recent SARS-CoV-2; and 1.0% (11/1148) in patients with previous SARS-CoV-2. After adjustment for confounding factors, patients with peri-operative (adjusted odds ratio 1.5 (95%CI 1.1-2.0)) and recent SARS-CoV-2 (1.9 (95%CI 1.2-3.3)) remained at higher risk of venous thromboembolism, with a borderline finding in previous SARS-CoV-2 (1.7 (95%CI 0.9-3.0)). Overall, venous thromboembolism was independently associated with 30-day mortality ). In patients with SARS-CoV-2, mortality without venous thromboembolism was 7.4% (319/4342) and with venous thromboembolism was 40.8% (31/76). Patients undergoing surgery with peri-operative or recent SARS-CoV-2 appear to be at increased risk of postoperative venous thromboembolism compared with patients with no history of SARS-CoV-2 infection. Optimal venous thromboembolism prophylaxis and treatment are unknown in this cohort of patients, and these data should be interpreted accordingly.

Segmental arterial mediolysis (SAM) is a rare but important cause of abdominal haemorrhage and is usually treated with endovascular management. Surgical or conservative management can be performed depending on the patient’s situation. Since the course of conservative treatment is not well described in the existing literature, it must be used with caution. We describe the case of a 52-year-old man who was transferred to the emergency department because of abdominal pain, diarrhoea, and haematemesis. On arrival, he was haemodynamically unstable, with a blood pressure of 70/40 mmHg. After he was transfused and stabilised in the emergency department, contrast-enhanced computed tomography (CECT) revealed a haematoma around the transverse colon and ascites, without any evident extravasation. The peripheral branch of the middle colic artery (MCA) showed irregular calibre, suggesting SAM. Since the patient remained stable, we initially chose conservative management. However, a CECT scan performed on the third day of hospitalisation showed coexisting pulmonary thromboembolism (PTE). Because of the need for anticoagulation therapy, we performed open surgery. The pathological examination was consistent with SAM. Anticoagulation therapy was initiated the next day. A CECT scan performed on a postoperative day (POD) 13 showed no PTE. Although the patient defecated haemorrhagic stool and experienced hematemesis on PODs 19 and 23, respectively, colonoscopy, esophagogastroduodenoscopy, and repeated CECT scans revealed no evidence of rebleeding, and no recurrence was observed. Open surgery produced a relatively good postoperative course for the patient. Endovascular management, however, remains a reasonable first approach, considering its reportedly excellent outcomes.

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Background While there are consensus recommendations for managing calcium channel blocker (CCB) toxicity, reports on angiotensin II receptor blocker (ARB) toxicity and management are limited. Herein, we report a case of catecholamine-refractory hypotension due to CCB and ARB overdose. Case presentation A 54-year-old woman with underlying hypertension was brought to the emergency department after she attempted suicide by ingesting 345 mg of amlodipine, a CCB, and 340 mg of olmesartan, an ARB. She was hypotensive, which was considered vasodilatory because of high cardiac and low systemic vascular resistance indices. Hypotension persisted despite the administration of norepinephrine and epinephrine. Intravenous calcium gluconate, glucagon, and high-dose insulin euglycemia therapy, which were initiated because CCB toxicity was suspected, failed to raise her blood pressure. The presence of normal anion-gap metabolic acidosis and the fact that the patient remained hypotensive suggested that the hypotension might have been due to the effect of ARB. Vasopressin was finally administered, which improved her hemodynamic status. She was weaned off all vasopressors on day 3. Discussion There is no consensus recommendation for ARB toxicity. Since chronic use of ARBs at conventional doses can block the sympathetic nervous and renin–angiotensin systems, catecholamines may not effectively increase blood pressure in cases of hypotension due to ARB overdose, for which vasopressin could be indicated. Conclusions Vasopressin could be an option for treating hypotension secondary to ARB and CCB toxicity when catecholamines and treatment for CCB toxicity fail.